First, we will further define the alterations in membrane permeability that occur after lectin treatment of lymphocytes. We will examine the role of a subtle increase in internal sodium (Na) (approximately 5mM) as the cause of an increased active transport rate of Na and potassium (K) in lymphocytes treated with lectins. We will 1) measure the Na content of lectin-treated lymphocytes, 2) determine the Na and K flux rates of untreated lymphocytes at an internal Na found in lectin-treated cells and 3) measure the kinetics of the transport-adenosine-triphosphatase of lymphocyte membrane vesicles for its cofactor Na. Second, we propose to define calcium (Ca) metabolism in lectin-treated and calcium-ionophore treated lymphocytes. These studies will measure the permeability, exchange and transport, of Ca by the membrane of cells and vesicles and isolated mitochondria. We will study the perturbation of Ca content, distribution and movement produced by lectin and ionophore treatment and correlate these with mitogenicity of these chemicals. Third, we plan to define the uptake of natural, neutral and amino acids by lymphocytes and characterize the alterations in membrane transport of natural amino acids induced by lectins or ionophores. In these studies, we propose to define the A and L-systems of amino acid transport and their alterations after perturbation by lectins or ionophores. Alterations in transport will be compared with the changes that occur when lymphocytes are exposed to amino acid deficient medium. We will determine if adaptation and lectin-induced enhanced amino acid uptake are similar. A vs. ASC vs. L-system amino acid uptake, kinetic parameters of uptake and sensitivity to metabolic inhibitors and glycocorticoids will be studied. We will define the differences in these membrane properties of human blood B and T lymphocytes.